The effect of metformin on blood pressure and metabolism in nondiabetic hypertensive patients

Snorgaard, Ole; Køber, Lars; Carlsen, Jens

doi:10.1046/j.1365-2796.1997.00236.x

Cited by 39 publications

(20 citation statements)

References 12 publications

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“…Administration of 500-850 mg metformin twice daily for 12 weeks lowered diastolic blood pressure in 25 nondiabetic hypertensive persons, but not significantly more than placebo did [40].…”

Section: Metformlnmentioning

confidence: 85%

A Review of Metabolic and Cardiovascular Effects of Oral Antidiabetic Agents: Beyond Glucose-Level Lowering

Ginsberg

Plutzky

Sobel

1999

European Journal of Cardiovascular Risk

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It has become evident that cardiovascular disease is the major cause of morbidity and mortality in type 2 diabetes mellitus. This raises the possibility that glucose lowering agents with other nonglucose-Iowering effects, might have added benefits. In this review, we focus on the metabolic and cardiovascular effects of oral antidiabetic agents that go beyond glucose-level lowering. Such effects include lipid modifying actions, antithrombotic and profibrinolytic activities, and direct action at the level of the vessel wall to improve endothelial function or prevent smooth muscle hyperplasia. These additional activities, particularly those seen with the newer oral antidiabetic agents, hold the promise of reducing cardiovascular complications beyond that achievable by glucose lowering alone. J Cardiovasc Risk 6:337-346

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“…Administration of 500-850 mg metformin twice daily for 12 weeks lowered diastolic blood pressure in 25 nondiabetic hypertensive persons, but not significantly more than placebo did [40].…”

Section: Metformlnmentioning

confidence: 85%

A Review of Metabolic and Cardiovascular Effects of Oral Antidiabetic Agents: Beyond Glucose-Level Lowering

Ginsberg

Plutzky

Sobel

1999

European Journal of Cardiovascular Risk

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“…In the literature, information is scarce regarding C peptide secretion after metformin treatment in groups of patients with normal glucose tolerance and insulin resistance (as women with PCOS mostly have). We are aware of a study (31) finding no change in either basal or stimulated levels of C peptide in a group of hypertensive patients after metformin. In a group of obese type 2 diabetics an increase in C peptide levels after metformin treatment was found (32).…”

Section: ) Although Not With Those Obtained By Others (12± 15)mentioning

confidence: 97%

The effects of long-term metformin treatment on adrenal and ovarian steroidogenesis in women with polycystic ovary syndrome

et al. 2001

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Objective: To evaluate adrenal and ovarian steroidogenesis before and after long-term treatment with metformin in women with polycystic ovary syndrome (PCOS). Design and Methods: Twenty-four women with PCOS were evaluated before and after treatment (27^4 weeks) with metformin (1000 mg/day) using adrenocorticotrophin (ACTH), GnRH analogue and oral glucose tolerance (oGTT) tests. For statistical evaluation, ANOVA and Wilcoxon's test were used. Results: In 58% of the women a significant improvement in menstrual cyclicity was observed. No significant change in basal steroid levels was found. After ACTH stimulation, a significant decrease in the activity of 3b-hydroxysteroid dehydrogenase in C 21 steroids P , 0X05 and in 17b-hydroxysteroid dehydrogenase P , 0X01 was observed, as was an increase in the activity of C17,20-lyase in the D 4 pathway P , 0X01X A significant growth in the dehydroepiandrosterone (DHEA)/DHEA-sulfate ratio P , 0X05 was detected. With regard to ovarian steroidogenesis, a significant decrease in the stimulated levels of testosterone P , 0X05Y index of free testosterone P , 0X01Y LH P , 0X05 and oestradiol P , 0X01Y and an increase in the levels of 17-hydroxypregnenolone P , 0X05 were detected. In the indices of ovarian enzyme activities, we observed a significant decrease in 3b-hydroxysteroid dehydrogenase in C 21 steroids P , 0X01Y in C17,20-lyase in the D5 pathway P , 0X01Y in 17b-hydroxysteroid dehydrogenase P , 0X05 and in aromatase. In glucose metabolism, a tendency towards reduction in the homeostasis model assessment (HOMA)-R (for insulin resistance) and HOMA-F (for b cell function) was detected. In addition, an increase in the levels of C peptide during oGTT was observed P , 0X01X Conclusions: Long-term metformin treatment reduced various steroid enzymatic activities both in the ovary and the adrenal glands, without apparent changes in basal steroid levels and in insulin sensitivity.

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“…Acta Pharmacologica Sinica npg effect on blood pressure in non-diabetic hypertensives [17] . We previously reported that metformin inhibited cardiac fibrosis in the TAC-mouse model and demonstrated that it inhibited collagen synthesis, likely via inhibition of the TGF-β 1 -Smad3 signaling pathway [18] .…”

Section: Wwwchinapharcom Fu Yn Et Almentioning

confidence: 99%

Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation

Xiao

et al. 2011

Acta Pharmacol Sin

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Aim: To identify the role of metformin in cardiac hypertrophy and investigate the possible mechanism underlying this effect. Methods: Wild type and AMPKα2 knockout (AMPKα2 -/-) littermates were subjected to left ventricular pressure overload caused by transverse aortic constriction. After administration of metformin (200 mg·kg -1 ·d -1 ) for 6 weeks, the degree of cardiac hypertrophy was evaluated using echocardiography and anatomic and histological methods. The antihypertrophic mechanism of metformin was analyzed using Western blotting. Results: Metformin significantly attenuated cardiac hypertrophy induced by pressure overload in wild type mice, but the antihypertrophic actions of metformin were ablated in AMPKα2 -/-mice. Furthermore, metformin suppressed the phosphorylation of Akt/protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in response to pressure overload in wild type mice, but not in AMPKα2 -/-mice. Conclusion: Long-term administration of metformin may attenuate cardiac hypertrophy induced by pressure overload in nondiabetic mice, and this attenuation is highly dependent on AMPK activation. These findings may provide a potential therapy for patients at risk of developing pathological cardiac hypertrophy.

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The effect of metformin on blood pressure and metabolism in nondiabetic hypertensive patients

Cited by 39 publications

References 12 publications

A Review of Metabolic and Cardiovascular Effects of Oral Antidiabetic Agents: Beyond Glucose-Level Lowering

A Review of Metabolic and Cardiovascular Effects of Oral Antidiabetic Agents: Beyond Glucose-Level Lowering

The effects of long-term metformin treatment on adrenal and ovarian steroidogenesis in women with polycystic ovary syndrome

Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation

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